Dr. Mark Haussler, PhD head shot

Contact Info

AZ Biomedical Collaborative 1
Room Number
Regents Professor Emeritus
College of Medicine Phx Basic Medical Sciences


  • Postdoctoral: Endocrine Signaling, University of Pennsylvania, 1968 – 1971.
  • PhD: University of California at Riverside, 1968.


  • Dampf Stone A, Batie SF,  Sabir MS,  Jacobs ET,  Lee JH,  Whitfield GK, Haussler MR and Jurutka PW. Resveratrol potentiates vitamin D and nuclear receptor signaling. J. Cellular Biochem. 116: 1130-1143 (2015). DOI 10.1002/jcb.25070. EPub 2014 Dec 25.
  • Kaneko I, Sabir MS, Dussik CM, Whitfield GK, Karrys A, Hsieh JC, Haussler MR, Meyer MB, Pike JW and Jurutka PW. 1,25-Dihydroxyvitamin D regulates expression of the tryptophan hydroxylase 2 and leptin genes: Implication for behavioral influences of vitamin D. FASEB J. 29: 4023-4035 (2015). DOI: 10.1096/fj.14-269811.
  • Kaneko I, Saini RK, Griffin KP, Whitfield GK, Haussler MR and Jurutka PW. FGF23 gene regulation by 1,25-dihydroxyvitamin D: opposing effects in adipocytes and osteocytes. J. Endocrinol. 226(3): 155-166 (2015). DOI: 10.1530/JOE-15-0225. EPub 6 July 2015.
  • Haussler MR, Whitfield GK, Haussler CA, Sabir MS, Khan Z, Sandoval R and Jurutka PW. 1,25-Dihydroxyvitamin D and klotho: a tale of two renal hormones coming of age. Chapter 8 in Vitamins and Hormones Volume 100, Gerald Litwack, ed., Elsevier, London, pp. 165-230 (2016).
  • Haussler MR, Saini RK, Sabir MS, Dussik CM, Khan Z, Whitfield GK, Griffin KP, Kaneko I and Jurutka PW. Vitamin D nutrient-gene interactions and healthful aging. Chapter 33 in Molecular Basis of Nutrition and Aging, First Edition, Marco Malavolta and Eugenio Mocchegiani, eds., Elsevier Academic Press, San Diego, pp. 449-471 (2016).

For a complete listing of Dr. Haussler's publications, search PubMed.

Research Interests

Vitamin D, nuclear receptors, healthy aging

Research Summary

We study how vitamin D, via the vitamin D receptor (VDR), decelerates chronic diseases of aging, such as osteoporosis and neurodegeneration. We hypothesize that 1,25-dihydroxyvitamin D (1,25D), through regulation of a novel bone-initiated FGF23/klotho/phosphate/CYP24A1 axis, prevents hyperphosphatemia and excessive concentrations of 1,25D, thereby slowing the onset of ectopic calcification, fibrosis, and vascular disease that can lead to kidney failure, myocardial infarction, and ischemic stroke.